Astragaloside IV alleviates the symptoms of experimental ulcerative colitis in vitro and in vivo
Affiliations: Department of Gastroenterology, Suzhou Municipal Integrated Traditional Chinese and Western Medicine Hospital, Suzhou, Jiangsu 215101, P.R. China
- Published online on: August 16, 2019 https://doi.org/10.3892/etm.2019.7907
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Ulcerative colitis (UC) is a chronic and relapsing inflammatory intestinal disease. Although the morbidity of UC has increased notably in recent years, effective therapeutic treatment remains unsatisfactory. Astragaloside IV (ASI), a monomeric compound isolated from the traditional Chinese medicine herb Ligusticum chuanxiong, exhibits anti‑inflammatory effects. The present study aimed to investigate the therapeutic effects of ASI on experimental UC in vitro and in vivo. Cell proliferation was detected via a Cell Counting Kit‑8 assay in vitro. In addition, the concentrations of the inflammatory factors myeloperoxidase (MPO), tumor necrosis factor‑α (TNF‑α), interleukin‑1β (IL‑1β), interleukin‑6 (IL‑6) and nitric oxide (NO) in the colon tissues were determined by ELISA. Western blot analysis was used to examine phosphorylated transcription factor p65 (p‑p65), p‑inhibitor of NF‑κB (IκB), claudin‑1 and tight junction protein ZO‑1 (ZO‑1) protein levels in vitro and in vivo, respectively. The results indicated that lipopolysaccharide (LPS) significantly increased the pro‑inflammatory cytokines TNF‑α, IL‑1β and IL‑6 in CCD‑18Co cells, which was markedly ameliorated by ASI. In addition to the inhibition of pro‑inflammatory cytokines, ASI decreased the levels of p‑p65 and p‑IκB proteins. In addition, ASI decreased the disease activity index scores, and increased colon lengths in dextran sulfate sodium‑induced UC mice. ASI also decreased the levels of the pro‑inflammatory factors MPO, TNF‑α, IL‑1β, IL‑6 and NO, and upregulated the expression of claudin‑1 and ZO‑1 in colon tissues. Therefore, ASI was effective in ameliorating experimental UC in vitro and in vivo via the inhibition of inflammatory molecules, and the downregulation of NF‑κB signaling. In conclusion, ASI may serve as a potential therapeutic agent for the treatment of UC.